Asset Details
Do you wish to reserve the book?
Decreased Fibronectin Production Significantly Contributes to Dysregulated Repair of Asthmatic Epithelium
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Decreased Fibronectin Production Significantly Contributes to Dysregulated Repair of Asthmatic Epithelium
Do you wish to request the book?
Decreased Fibronectin Production Significantly Contributes to Dysregulated Repair of Asthmatic Epithelium
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Decreased Fibronectin Production Significantly Contributes to Dysregulated Repair of Asthmatic Epithelium
2010
Overview
Damage to airway epithelium is followed by deposition of extracellular matrix (ECM) and migration of adjacent epithelial cells. We have shown that epithelial cells from children with asthma fail to heal a wound in vitro.
To determine whether dysregulated ECM production by the epithelium plays a role in aberrant repair in asthma.
Airway epithelial cells (AEC) from children with asthma (n = 36), healthy atopic control subjects (n = 23), and healthy nonatopic control subjects (n = 53) were investigated by microarray, gene expression and silencing, transcript regulation analysis, and ability to close mechanical wounds.
Time to repair a mechanical wound in vitro by AEC from healthy and atopic children was not significantly different and both were faster than AEC from children with asthma. Microarray analysis revealed differential expression of multiple gene sets associated with repair and remodeling in asthmatic AEC. Fibronectin (FN) was the only ECM component whose expression was significantly lower in asthmatic AEC. Expression differences were verified by quantitative polymerase chain reaction and ELISA, and reduced FN expression persisted in asthmatic cells over passage. Silencing of FN expression in nonasthmatic AEC inhibited wound repair, whereas addition of FN to asthmatic AEC restored reparative capacity. Asthmatic AEC failed to synthesize FN in response to wounding or cytokine/growth factor stimulation. Exposure to 5', 2'deoxyazacytidine had no effect on FN expression and subsequent analysis of the FN promoter did not show evidence of DNA methylation.
These data show that the reduced capacity of asthmatic epithelial cells to secrete FN is an important contributor to the dysregulated AEC repair observed in these cells.
Publisher
American Thoracic Society,Oxford University Press
Subject
/ Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy
/ Asthma
/ Biological and medical sciences
/ Child
/ Cycloheximide - pharmacology
/ Dexamethasone - pharmacology
/ Enzyme-Linked Immunosorbent Assay
/ Epithelial Cells - drug effects
/ Epithelial Cells - physiology
/ Extracellular Matrix - metabolism
/ Humans
/ Hydroxamic Acids - pharmacology
/ Hypersensitivity - physiopathology
/ Local anesthesia. Pain (treatment)
/ Respiratory Mucosa - physiopathology
